Dissecting the regulatory landscape of the<i>Abd-B</i>gene of the bithorax complex

Mihály, József; Barges, Stéphane; Sípos, László; Maeda, Robert K.; Cléard, Fabienne; Hogga, Iiham; Bender, Welcome; Gyurkovics, Henrik; Karch, François

doi:10.1242/dev.02451

Cited by 82 publications

(119 citation statements)

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“…1A). And third, recent data have suggested that BX-C boundaries are regulated along the AP axis (Cléard et al, 2006). From these data, it seems that boundaries interact with the Abd-B promoter until the neighboring (probably more posterior) domain becomes active (see also Maeda and Karch, 2007).…”

Section: Resultsmentioning

confidence: 94%

“…The iab-6 enhancer region controls the level of Abd-B expression in parasegment 11 (PS11) and determines the identity of segment A6. The iab-7 region, however, controls the level of Abd-B expression in PS12 and determines the identity of segment A7 (Celniker et al, 1990;Galloni et al, 1993;Mihaly et al, 2006;Sanchez-Herrero, 1991). When Fab-7 is deleted, the iab-6 and iab-7 domains become fused into a single domain, allowing both the iab-6 and iab-7 enhancers or silencers to become active in PS11 and PS12.…”

Section: Introductionmentioning

confidence: 99%

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Boundary swapping in theDrosophilaBithorax complex

et al. 2008

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Although the boundary elements of the Drosophila Bithorax complex (BX-C) have properties similar to chromatin insulators, genetic substitution experiments have demonstrated that these elements do more than simply insulate adjacent cis-regulatory domains. Many BX-C boundaries lie between enhancers and their target promoter, and must modulate their activity to allow distal enhancers to communicate with their target promoter. Given this complex function, it is surprising that the numerous BX-C boundaries share little sequence identity. To determine the extent of the similarity between these elements, we tested whether different BX-C boundary elements can functionally substitute for one another. Using gene conversion, we exchanged the Fab-7 and Fab-8 boundaries within the BX-C. Although the Fab-8 boundary can only partially substitute for the Fab-7 boundary, we find that the Fab-7 boundary can almost completely replace the Fab-8 boundary. Our results suggest that although boundary elements are not completely interchangeable, there is a commonality to the mechanism by which boundaries function. This commonality allows different DNA-binding proteins to create functional boundaries.

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Section: Resultsmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 99%

Boundary swapping in theDrosophilaBithorax complex

et al. 2008

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“…Thus the Abd-Bm expression anterior to A8 occurs at a time when the cells are refractory to posterior spiracle induction (Castelli-Gair, (iab), capable of driving expression in the Abd-B domain. iab elements are flanked by Fab boundary elements required to isolate their domains of action (Barges et al, 2000, Mihaly et al, 2006, Zhou et al, 1996. Of particular relevance for spiracle development are a 3' iab-8 and a 5' iab-8 element able to drive expression in the A8 segment from stage 9 (Estrada et al, 2002).…”

Section: Abd-b Transcriptional Regulationmentioning

confidence: 99%

Genetic control of morphogenesis - Hox induced organogenesis of the posterior spiracles

Hombría¹,

Rivas²,

Sotillos³

2009

Int. J. Dev. Biol.

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The posterior spiracle has become one of the best systems to study how Hox genes control morphogenesis. Interaction of Abdominal-B (ABD-B) with dorso ventral and intrasegmental positional information leads to the local activation of ABD-B primary targets in the dorsal region of the eighth abdominal segment (A8). Primary targets pattern the spiracle subdividing it into two broad areas: external stigmatophore vs. internal spiracular chamber precursor cells. Primary targets then activate secondary targets and modulate the expression of signalling molecules in the spiracle primordium creating unique spiracle positional values. This genetic cascade activates the "realisator" genes that modulate the cell behaviours causing invagination, elongation and cell rearrangements responsible for spiracle morphogenesis. The spiracle realisators that have been identified to date correspond to cell adhesion proteins, cytoskeleton regulators and cell polarity molecules. Interestingly, these realisators localise to different apico-basal locations in the cell (RhoGEF apical, Crumbs subapical, E-cadherin in the adherens junction, RhoGAP basolateral). Therefore, the Hox anterior-posterior code is converted in the cell into apico-basal information required to implement the posterior spiracle morphogenetic program. We believe this may be a common characteristic for Hox induced organogenesis. KEY WORDS: posterior spiracles, ABD-B, Hox gene, morphogenesis, organogenesisHow undifferentiated cells make an organ in a precise location is one of the key questions in Developmental Biology. While certain organs are repeatedly formed along the body axis, others are localised in particular antero-posterior positions by the control of the transcription factors encoded by the Hox genes (also known as homeotic genes). Hox genes activate stable developmental programs that allow the formation of segment specific structures. These structures may consist of particular bones with their unique shapes or of specific organs. An example of Hox gene regulation in mammals is the skeletal structure with its variety of vertebrae shapes and associated ribs. A similar example in arthropods is the variety of leg appendages present along the anterior-posterior axis of the body. In the past fifteen years our laboratory has analysed the posterior spiracles of Drosophila as a model to understand how the morphogenesis of segment specific organs is controlled. Our studies range from the early primordium specification to its final differentiation, trying to find out how the specific behaviour of groups of cells is integrated to achieve the morphogenetic movements that shape the organ. This review summarizes the work of our laboratory and others in what is one of the most Int. J. Dev. Biol. 53: 1349-1358 (2009) Posterior spiracle development overviewThe posterior spiracles form the only external connexion of the tracheal respiratory system of the early Drosophila larva. The posterior spiracles are ectoderm-derived epithelial structures composed of two differe...

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“…Genetic and molecular studies have shown that each of these regulatory domains is bracketed by boundary elements Mcp, and AB-I; Fig. 1A) (Celniker et al, 1990;Gyurkovics et al, 1990;Galloni et al, 1993;Karch et al, 1994;Kyrchanova et al, 2008Kyrchanova et al, , 2011Kyrchanova et al, , 2016McCall et al, 1994;Mihaly et al, 1997Mihaly et al, , 2006Barges et al, 2000;Iampietro et al, 2010;Bender and Lucas, 2013;Bowman et al, 2014). BX-C boundaries have two important functions : one is to block crosstalk between adjacent regulatory domains; the other is bypass activity, i.e.…”

Section: Introductionmentioning

confidence: 99%

Architectural protein Pita cooperates with dCTCF in organization of functional boundaries in Bithorax complex

et al. 2017

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Boundaries in the Bithorax complex (BX-C) of Drosophila delimit autonomous regulatory domains that drive parasegment-specific expression of homeotic genes. BX-C boundaries have two crucial functions: they must block crosstalk between adjacent regulatory domains and at the same time facilitate boundary bypass. The C2H2 zinc-finger protein Pita binds to several BX-C boundaries, including Fab-7 and Mcp. To study Pita functions, we have used a boundary replacement strategy by substituting modified DNAs for the Fab-7 boundary, which is located between the iab-6 and iab-7 regulatory domains. Multimerized Pita sites block iab-6↔iab-7 crosstalk but fail to support iab-6 regulation of Abd-B (bypass). In the case of Fab-7, we used a novel sensitized background to show that the two Pita-binding sites contribute to its boundary function. Although Mcp is from BX-C, it does not function appropriately when substituted for Fab-7: it blocks crosstalk but does not support bypass. Mutation of the Mcp Pita site disrupts blocking activity and also eliminates dCTCF binding. In contrast, mutation of the Mcp dCTCF site does not affect Pita binding, and this mutant boundary retains partial function.

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Dissecting the regulatory landscape of theAbd-Bgene of the bithorax complex

Cited by 82 publications

References 58 publications

Boundary swapping in theDrosophilaBithorax complex

Boundary swapping in theDrosophilaBithorax complex

Genetic control of morphogenesis - Hox induced organogenesis of the posterior spiracles

Architectural protein Pita cooperates with dCTCF in organization of functional boundaries in Bithorax complex

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